Expression profile of miRNA in NSCLC tissues in middle-altitude area

中海拔地区NSCLC组织中miRNA的表达谱

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作者:Yuhai Gu, Xuefeng Shi, Xinying Wang, Xia Liu, Youbang Xie

Abstract

Micro ribonucleic acid (miRNA) expression profile in non-small cell lung cancer (NSCLC) tissues in middle-altitude area was analyzed using the Affymetrix chip technique, to predict the target genes of abnormally-expressed miRNAs, and to analyze the target gene-related signaling pathways and cell biological functions regulated by them. The difference in miRNA expression profile in NSCLC tissues was analyzed using the Affymetrix chip technique. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed for the verification of some differentially-expressed miRNAs. The genes predicted by at least 6 out of 12 commonly used prediction methods of miRNA target genes, based on miRWalk2.0, were considered as target genes. The functions of differentially-expressed miRNA target genes were analyzed via Gene Ontology (GO) enrichment analysis, and the main signaling pathways involving target genes were analyzed via Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. There was abnormal expression of miRNAs in NSCLC tissues in the middle-altitude area. There were 140,405 target genes predicted for differentially-expressed miRNAs. The GO enrichment analysis of the functions of the target genes of differentially expressed miRNAs revealed that they mainly influence the binding process of intracellular components to protein, the positive regulation of biological process and the regulation of metabolic process. Moreover, these target genes were mainly enriched in the immunity, gene expression, metabolism and signal transduction, among which signal transduction was enriched with the most genes. The expression levels of miRNA-139-5p and miRNA-150-5p in lung cancer group were lower than those in the control group. The expression of miRNAs in NSCLC tissues in the middle-altitude area is abnormal, and most miRNAs are downregulated.

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